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Article: Focus on antioxidant enzymes and antioxidant strategies in smoking related airway diseases.

Kinnula, V L

2005 Volume 60, Issue 8, Page(s) 693–700

Abstract: Cigarette smoke causes significant oxidant stress which is further enhanced by recruitment and activation of inflammatory cells to the lung. Polymorphisms in some detoxification enzymes are thought to increase the risk of developing chronic obstructive ... ...

Abstract	Cigarette smoke causes significant oxidant stress which is further enhanced by recruitment and activation of inflammatory cells to the lung. Polymorphisms in some detoxification enzymes are thought to increase the risk of developing chronic obstructive pulmonary disease (COPD), but the ultimate role of genetic variability in antioxidant and/or detoxification enzymes in COPD remains obscure. Some antioxidant enzymes are inducted, but the extent of induction is insufficient to protect the lung/alveolar epithelium against cigarette smoke. Exogenous antioxidants such as vitamins do not seem to protect against cigarette smoke related lung injury. Glutathione related synthetic drugs such as N-acetylcysteine have shown some benefits, but they may have pro-oxidant side effects. Synthetic compounds with superoxide dismutase and catalase activities have shown promising results in animal models against a variety of oxidant exposures including cigarette smoke in the lung. These results are in agreement with studies highlighting the importance of alveolar antioxidant protection mechanisms in oxidant stress and their inducibility. These new drugs need to be tested in cigarette smoking related lung injury/inflammation since inflammation/oxidant stress can continue after discontinuation of smoking.
MeSH term(s)	Antioxidants/metabolism ; Antioxidants/therapeutic use ; Humans ; Hydrogen Peroxide/metabolism ; Lung Diseases/enzymology ; Lung Diseases/genetics ; Oxidative Stress/genetics ; Oxidative Stress/physiology ; Polymorphism, Genetic ; Pulmonary Disease, Chronic Obstructive/enzymology ; Pulmonary Disease, Chronic Obstructive/genetics ; Reactive Oxygen Species/metabolism ; Smoking/adverse effects ; Superoxide Dismutase/metabolism
Chemical Substances	Antioxidants ; Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2005-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	204353-1
ISSN	1468-3296 ; 0040-6376
ISSN (online)	1468-3296
ISSN	0040-6376
DOI	10.1136/thx.2004.037473
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Article: Oxidant and antioxidant mechanisms of lung disease caused by asbestos fibres.

Kinnula, V L

The European respiratory journal

1999 Volume 14, Issue 3, Page(s) 706–716

Abstract: The pathogenesis of asbestos-related lung diseases is complicated and still poorly understood. Studies on animal models and cell cultures have indicated that asbestos fibres generate reactive oxygen and nitrogen species and cause oxidation and/or ... ...

Abstract	The pathogenesis of asbestos-related lung diseases is complicated and still poorly understood. Studies on animal models and cell cultures have indicated that asbestos fibres generate reactive oxygen and nitrogen species and cause oxidation and/or nitrosylation of proteins and deoxyribonucleic acid as a marker of cell injury. These effects are potentiated by the inflammation caused by the fibres. Recent studies have shown that individual variability in the antioxidant and/or detoxifying mechanisms probably has an important role in the development of asbestos-related lung diseases. Asbestos fibres cause both cell proliferation and apoptosis by multiple mechanisms, one of them being activation of signal transduction pathways by reactive oxygen and nitrogen species. Asbestos activates transcription factors such as nuclear factor kappa B, which has been shown to lead to the upregulation of antioxidant enzymes, most importantly manganese superoxide dismutase. This enzyme is also overexpressed in asbestos-related human malignant mesothelioma, whereas the induction of other antioxidant enzymes (copper-zinc superoxide dismutase, catalase, glutathione peroxidase) by asbestos fibres appears to be marginal. The significance of antioxidant enzymes in asbestos related diseases has, however, remained unclear. Furthermore, previous studies have not been able to offer successful therapies to the patients with asbestos-associated diseases. Only an improved understanding of the pathogenetic mechanisms in the human lung provides a basis for future therapies for asbestos-related diseases.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Antioxidants/therapeutic use ; Apoptosis/genetics ; Asbestos/adverse effects ; Asbestosis/etiology ; Asbestosis/metabolism ; Asbestosis/pathology ; Asbestosis/prevention & control ; Cell Division/drug effects ; Cell Division/genetics ; DNA Damage/drug effects ; Humans ; Nitrogen Oxides/metabolism ; Oxidation-Reduction/drug effects ; Reactive Oxygen Species/metabolism
Chemical Substances	Antioxidants ; Nitrogen Oxides ; Reactive Oxygen Species ; Asbestos (1332-21-4)
Language	English
Publishing date	1999-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1034/j.1399-3003.1999.14c35.x
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Article: Keuhkosolujen oksidatiivisista ja antioksidatiivisista ominaisuuksista.

Kinnula, V L

Duodecim; laaketieteellinen aikakauskirja

1992 Volume 108, Issue 14, Page(s) 1246–1252

Title translation	Oxidant and antioxidant properties of lung cells.
MeSH term(s)	Acetylcysteine/therapeutic use ; Antioxidants/metabolism ; Endothelium/metabolism ; Glutathione/therapeutic use ; Glutathione Peroxidase/metabolism ; Humans ; Lung/cytology ; Lung/metabolism ; Oxidants/metabolism ; Pulmonary Alveoli/metabolism ; Vitamins/therapeutic use
Chemical Substances	Antioxidants ; Oxidants ; Vitamins ; Glutathione Peroxidase (EC 1.11.1.9) ; Glutathione (GAN16C9B8O) ; Acetylcysteine (WYQ7N0BPYC)
Language	Finnish
Publishing date	1992
Publishing country	Finland
Document type	Journal Article ; Review
ZDB-ID	127604-9
ISSN	0012-7183
ISSN	0012-7183
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Article ; Online: SIRT1 as a therapeutic target in inflammaging of the pulmonary disease.

Rahman, Irfan / Kinnula, Vuokko L / Gorbunova, Vera / Yao, Hongwei

Preventive medicine

2011 Volume 54 Suppl, Page(s) S20–8

Abstract: Objective: Chronic inflammation and cellular senescence are intertwined in the pathogenesis of premature aging, which is considered as an important contributing factor in driving chronic obstructive pulmonary disease (COPD). Sirtuin1 (SIRT1), a ... ...

Abstract	Objective: Chronic inflammation and cellular senescence are intertwined in the pathogenesis of premature aging, which is considered as an important contributing factor in driving chronic obstructive pulmonary disease (COPD). Sirtuin1 (SIRT1), a nicotinamide adenine dinucleotide (NAD(+))-dependent protein/histone deacetylase, regulates inflammation, senescence/aging, stress resistance, and deoxyribonucleic acid (DNA) damage repair via deacetylating intracellular signaling molecules and chromatin histones. The present review describes the mechanism and regulation of SIRT1 by environmental agents/oxidants/reactive aldehydes and pro-inflammatory stimuli in lung inflammation and aging. The role of dietary polyphenols in regulation of SIRT1 in inflammaging is also discussed. Methods: Analysis of current research findings on the mechanism of inflammation and senescence/aging (i.e., inflammaging) and their regulation by SIRT1 in premature aging of the lung. Results: COPD is a disease of the lung inflammaging, which is associated with the DNA damage response, transcription activation and chromatin modifications. SIRT1 regulates inflammaging via regulating forkhead box class O 3, p53, nuclear factor kappa B, histones and various proteins involved in DNA damage and repair. Polyphenols and its analogs have been shown to activate SIRT1 although they have anti-inflammatory and antioxidant properties. Conclusions: Targeting lung inflammation and cellular senescence as well as premature lung aging using pharmacological SIRT1 activators or polyphenols would be a promising therapeutic intervention for COPD/emphysema.
MeSH term(s)	Aging, Premature/metabolism ; Cellular Senescence/physiology ; DNA Damage ; Humans ; Oxidative Stress ; Polyphenols/pharmacology ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Pulmonary Emphysema/drug therapy ; Sirtuin 1/drug effects ; Sirtuin 1/metabolism ; Sirtuin 1/therapeutic use
Chemical Substances	Polyphenols ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2011-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184600-0
ISSN	1096-0260 ; 0091-7435
ISSN (online)	1096-0260
ISSN	0091-7435
DOI	10.1016/j.ypmed.2011.11.014
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Article ; Online: Nitric oxide-induced eosinophil apoptosis is dependent on mitochondrial permeability transition (mPT), JNK and oxidative stress: apoptosis is preceded but not mediated by early mPT-dependent JNK activation.

Ilmarinen-Salo, Pinja / Moilanen, Eeva / Kinnula, Vuokko L / Kankaanranta, Hannu

Respiratory research

2012 Volume 13, Page(s) 73

Abstract: ... content, by Annexin-V labelling and/or morphological analysis. Immunoblotting was used to study phospho ... measures analysis of variance (ANOVA) or paired t-test.: Results: NO-donor S-nitroso-N-acetyl-D,L ...

Abstract	Background: Eosinophils are critically involved in the pathogenesis of asthma. Nitric oxide (NO) is produced in high amounts in asthmatic lungs and has an important role as a regulator of lung inflammation. NO was previously shown to induce eosinophil apoptosis mediated via c-jun N-terminal kinase (JNK) and caspases. Our aim was to clarify the cascade of events leading to NO-induced apoptosis in granulocyte macrophage-colony stimulating factor (GM-CSF)-treated human eosinophils concentrating on the role of mitochondria, reactive oxygen species (ROS) and JNK. Methods: Apoptosis was determined by flow cytometric analysis of relative DNA content, by Annexin-V labelling and/or morphological analysis. Immunoblotting was used to study phospho-JNK (pJNK) expression. Mitochondrial membrane potential was assessed by JC-1-staining and mitochondrial permeability transition (mPT) by loading cells with calcein acetoxymethyl ester (AM) and CoCl2 after which flow cytometric analysis was conducted. Statistical significance was calculated by repeated measures analysis of variance (ANOVA) or paired t-test. Results: NO-donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) induced late apoptosis in GM-CSF-treated eosinophils. SNAP-induced apoptosis was suppressed by inhibitor of mPT bongkrekic acid (BA), inhibitor of JNK SP600125 and superoxide dismutase-mimetic AEOL 10150. Treatment with SNAP led to late loss of mitochondrial membrane potential. Additionally, we found that SNAP induces early partial mPT (1 h) that was followed by a strong increase in pJNK levels (2 h). Both events were prevented by BA. However, these events were not related to apoptosis because SNAP-induced apoptosis was prevented as efficiently when BA was added 16 h after SNAP. In addition to the early and strong rise, pJNK levels were less prominently increased at 20-30 h. Conclusions: Here we demonstrated that NO-induced eosinophil apoptosis is mediated via ROS, JNK and late mPT. Additionally, our results suggest that NO induces early transient mPT (flickerings) that leads to JNK activation but is not significant for apoptosis. Thereby, we showed some interesting early events in NO-stimulated eosinophils that may take place even if the threshold for irreversible mPT and apoptosis is not crossed. This study also revealed a previously unknown physiological function for transient mPT by showing that it may function as initiator of non-apoptotic JNK signalling.
MeSH term(s)	Apoptosis/drug effects ; Apoptosis/physiology ; Asthma/metabolism ; Asthma/physiopathology ; Eosinophils/drug effects ; Eosinophils/metabolism ; Eosinophils/pathology ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Humans ; MAP Kinase Kinase 4/drug effects ; MAP Kinase Kinase 4/metabolism ; Membrane Potential, Mitochondrial/drug effects ; Membrane Potential, Mitochondrial/physiology ; Mitochondria/drug effects ; Mitochondria/physiology ; Nitric Oxide/pharmacology ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; S-Nitroso-N-Acetylpenicillamine/pharmacology ; Signal Transduction/drug effects
Chemical Substances	Reactive Oxygen Species ; Nitric Oxide (31C4KY9ESH) ; S-Nitroso-N-Acetylpenicillamine (79032-48-7) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; MAP Kinase Kinase 4 (EC 2.7.12.2)
Language	English
Publishing date	2012-08-24
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-9921
ISSN (online)	1465-993X
ISSN	1465-9921
DOI	10.1186/1465-9921-13-73
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Article: Endogenous antioxidant enzymes and glutathione S-transferase in protection of mesothelioma cells against hydrogen peroxide and epirubicin toxicity.

Kinnula, K / Linnainmaa, K / Raivio, K O / Kinnula, V L

British journal of cancer

1998 Volume 77, Issue 7, Page(s) 1097–1102

Abstract: We have previously shown that cultured malignant mesothelioma cells contain elevated manganese superoxide dismutase (MnSOD) mRNA levels and activities compared with non-malignant mesothelial cells. As many cytotoxic drugs generate both superoxide and ... ...

Abstract	We have previously shown that cultured malignant mesothelioma cells contain elevated manganese superoxide dismutase (MnSOD) mRNA levels and activities compared with non-malignant mesothelial cells. As many cytotoxic drugs generate both superoxide and hydrogen peroxide, we assessed the relative significance of catalase and the glutathione redox cycle, as well as glutathione S-transferase (GST), in protecting these cells against hydrogen peroxide and epirubicin toxicity. Mesothelioma cell lines containing high (M38K cells) and low (M14K cells) MnSOD, and non-malignant MeT-5A mesothelial cells were selected for the study. M38K cells were the most resistant of these three cell types to hydrogen peroxide (0.1-0.5 mM, 4 h) and epirubicin (0.1-0.5 microg ml(-1), 48 h) as judged by lactate dehydrogenase (LDH) release and by high-energy nucleotide (ATP, ADP, AMP) depletion. Total glutathione was higher in M38K cells (63.8 +/- 20.3 nnmol mg(-1) protein) than in M14K (25.2 +/- 8.2 nmol mg[-1]) or MeT-5A cells (23.5 +/- 4.5 nmol mg[-1]). Furthermore, GST specific activity was higher in M38K cells (111.3 +/- 15.8 U mg[-1]) than in M14K cells (77.4 +/- 6.6 U mg[-1]) or in MeT-5A cells (68.8 +/- 7.6 U mg[-1]). Western blotting indicated the presence of GST-pi in all these cells, the reactivity again being highest in M38K cells. Depletion of glutathione by buthionine sulphoximine and inhibition of catalase by aminotriazole enhanced hydrogen peroxide toxicity in all cell types, while only the depletion of glutathione increased epirubicin toxicity. We conclude that simultaneous induction of multiple antioxidant enzymes can occur in human mesothelioma cells. In addition to the high MnSOD activity, hydrogen peroxide scavenging antioxidant enzymes, glutathione and GST can partly explain the high hydrogen peroxide and epirubicin resistance of these cells in vitro.
MeSH term(s)	Antibiotics, Antineoplastic/pharmacology ; Antioxidants/metabolism ; Epirubicin/pharmacology ; Glutathione Transferase/drug effects ; Glutathione Transferase/metabolism ; Humans ; Hydrogen Peroxide/pharmacology ; Mesothelioma/enzymology ; Mesothelioma/metabolism ; Oxidants/pharmacology ; Tumor Cells, Cultured/drug effects
Chemical Substances	Antibiotics, Antineoplastic ; Antioxidants ; Oxidants ; Epirubicin (3Z8479ZZ5X) ; Hydrogen Peroxide (BBX060AN9V) ; Glutathione Transferase (EC 2.5.1.18)
Language	English
Publishing date	1998-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/bjc.1998.182
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Article: Hyperventilation during exercise: independence on exercise-induced bronchoconstriction in mild asthma.

Kinnula, V L / Sovijärvi, A R

Respiratory medicine

1996 Volume 90, Issue 3, Page(s) 145–151

Abstract: Ventilatory gas exchange during exercise was compared in patients with mild asthma (11 females and 11 males), hyperventilation syndrome (HVS, 11 females), and healthy subjects (11 females and 11 males) in order to assess hyperventilation during exercise ... ...

Abstract	Ventilatory gas exchange during exercise was compared in patients with mild asthma (11 females and 11 males), hyperventilation syndrome (HVS, 11 females), and healthy subjects (11 females and 11 males) in order to assess hyperventilation during exercise and its association with exercise-induced bronchoconstriction. The asthmatics showed decreased working capacity and decreased maximal oxygen consumption, with no evidence of limitation due to impairment of ventilatory capacity. Ventilatory equivalents for CO2 and O2 (VE/VCO2 and VE/VO2) at rest did not differ between the controls and asthmatics, but they were significantly elevated in HVS. In female asthmatics, ventilatory equivalents during exercise were significantly (P < 0.05) elevated compared with those of healthy subjects; in female controls, VE/VCO2 was 30.1 +/- 3.3 at low exercise and 27.4 +/- 6.5 at maximal exercise. In female asthmatics, the corresponding figures were 34.9 +/- 6.1 and 36.7 +/- 5.3. Furthermore, VE/VCO2 individually related to percent of maximal oxygen consumption (VO2max) was significantly increased in female asthmatics both at low and high VO2. The highest ventilatory equivalents were obtained in HVS, 41.7 +/- 6.7 and 43.9 +/- 0.9, respectively. Significant exercise-induced bronchoconstriction (decrease of FEV1 > 15%) was found in 50% of the asthmatics. The ventilatory equivalents did not correlate with exercise-induced changes in FEV1 (r2 < 0.3). Mild exercise-induced hyperventilation which was observed in mild female asthmatics, did not appear to be related to exercise-induced bronchoconstriction.
MeSH term(s)	Adult ; Asthma, Exercise-Induced/metabolism ; Asthma, Exercise-Induced/physiopathology ; Bronchoconstriction ; Exercise ; Female ; Forced Expiratory Volume ; Humans ; Hyperventilation/metabolism ; Hyperventilation/physiopathology ; Hyperventilation/psychology ; Lung/physiopathology ; Male ; Oxygen Consumption/physiology ; Pulmonary Gas Exchange
Language	English
Publishing date	1996-03
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	1003348-8
ISSN	1532-3064 ; 0954-6111
ISSN (online)	1532-3064
ISSN	0954-6111
DOI	10.1016/s0954-6111(96)90156-0
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Article ; Online: Successful Smoking Cessation in COPD: Association with Comorbidities and Mortality.

Kupiainen, H / Kinnula, V L / Lindqvist, A / Postma, D S / Boezen, H M / Laitinen, T / Kilpeläinen, M

Pulmonary medicine

2012 Volume 2012, Page(s) 725024

Abstract: Smoking cessation is the cornerstone of COPD management, but difficult to achieve in clinical practice. The effect of comorbidities on smoking cessation and risk factors for mortality were studied in a cohort of 739 COPD patients recruited in two Finnish ...

Abstract	Smoking cessation is the cornerstone of COPD management, but difficult to achieve in clinical practice. The effect of comorbidities on smoking cessation and risk factors for mortality were studied in a cohort of 739 COPD patients recruited in two Finnish University Hospitals. The diagnosis of COPD was done for the first time on average 5.5 years prior to the enrollment. Data from the medical records and followup questionnaires (years 0, 1, 2, and 4) have been analyzed. The patients' lung function varied greatly; mean FEV(1) 58% of predicted. A total of 60.2% of men and 55.6% of women had been able to quit smoking. Alcohol abuse (OR 2.1, 95% CI 1.4-3.3) and psychiatric conditions (OR 1.8, 95% CI 1.2-2.7) were strongly related to low success rates of quitting. Among current smokers high nicotine dependency was again explained by alcohol abuse and psychiatric conditions. Non-quitters were younger than quitters, but their mortality rates remained significantly higher even when the model was adjusted for impairment of lung functions and comorbidities. In conclusion, co-existing addiction and psychiatric diseases significantly decreased the success rates in smoking cessation and increased mortality among the patients.
Language	English
Publishing date	2012-11-14
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2603580-7
ISSN	2090-1844 ; 2090-1844
ISSN (online)	2090-1844
ISSN	2090-1844
DOI	10.1155/2012/725024
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Article ; Online: Elevation of surfactant protein A in plasma and sputum in cigarette smokers.

Mazur, W / Toljamo, T / Ohlmeier, S / Vuopala, K / Nieminen, P / Kobayashi, H / Kinnula, V L

The European respiratory journal

2011 Volume 38, Issue 2, Page(s) 277–284

Abstract: Serum surfactant protein (SP)-A has been postulated to associate with pulmonary fibrosis, but its role in cigarette smoking-related lung diseases is undefined. SP-A levels in plasma and induced sputum in nonsmokers, smokers with respiratory symptoms ( ... ...

Abstract	Serum surfactant protein (SP)-A has been postulated to associate with pulmonary fibrosis, but its role in cigarette smoking-related lung diseases is undefined. SP-A levels in plasma and induced sputum in nonsmokers, smokers with respiratory symptoms (cough and/or phlegm) and symptom-free smokers were assessed using a validated EIA method. A total of 474 current smokers without any diseases or medications were enrolled and followed for 2 yrs with 111 of them succeeding in stopping. Plasma SP-A level was detectable in all subjects and elevated in smokers independently of the symptoms compared to nonsmokers (p = 0.001). After 2 yrs of follow-up, the SP-A level was higher in those who continued smoking compared to the quitters (p<0.001). Plasma SP-A levels were associated with age, smoking history and lung function. Sputum (n = 109) SP-A was nondetectable in most nonsmokers, whereas smoking and symptoms increased sputum SP-A highly significantly (p = 0.001). In conclusion, SP-A may be involved in pathogenesis of cigarette smoking-related lung diseases. Further studies are needed to elucidate the role of SP-A in chronic obstructive pulmonary disease.
MeSH term(s)	Age Factors ; Aged ; Cough/chemically induced ; Cough/physiopathology ; Female ; Humans ; Longitudinal Studies ; Lung/physiopathology ; Male ; Middle Aged ; Pulmonary Surfactant-Associated Protein A/blood ; Respiratory Function Tests ; Smoking/blood ; Smoking Cessation ; Sputum/chemistry
Chemical Substances	Pulmonary Surfactant-Associated Protein A
Language	English
Publishing date	2011-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/09031936.00110510
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Article: Elevated ventilatory equivalents during exercise in patients with hyperventilation syndrome.

Kinnula, V L / Sovijärvi, A R

Respiration; international review of thoracic diseases

1993 Volume 60, Issue 5, Page(s) 273–278

Abstract: In hyperventilation syndrome (HVS), hyperventilation is often provoked by exercise. This study was undertaken to investigate gas exchange parameters and their correlation to arterial blood gas values in HVS patients during exercise. Ventilatory ... ...

Abstract	In hyperventilation syndrome (HVS), hyperventilation is often provoked by exercise. This study was undertaken to investigate gas exchange parameters and their correlation to arterial blood gas values in HVS patients during exercise. Ventilatory equivalents for oxygen (VE/VO2) and carbon dioxide (VE/VCO2) were significantly higher in HVS patients than in the controls. (VE/VO2) during light exercise (40-50 W) was 23.1 +/- 2.7 (n = 10) in the controls and 35.2 +/- 8.2 (n = 10) in the HVS group (p < 0.01). VE/VCO2 during light exercise was 30.0 +/- 3.3 in the controls and 41.8 +/- 6.0 in the HVS group (p < 0.01). In HVS, significantly correlations were observed between VE/VCO2 and PaCO2, and between VE/VO2 and PaCO2 during both light and maximal exercise (p < 0.02). The findings suggest that exercise testing can be used to aid HVS diagnosis without invasive arterial cannulation.
MeSH term(s)	Adult ; Carbon Dioxide/blood ; Exercise Test ; Female ; Humans ; Hyperventilation/diagnosis ; Hyperventilation/physiopathology ; Male ; Middle Aged ; Oxygen/blood ; Respiration/physiology
Chemical Substances	Carbon Dioxide (142M471B3J) ; Oxygen (S88TT14065)
Language	English
Publishing date	1993
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	206674-9
ISSN	1423-0356 ; 0025-7931
ISSN (online)	1423-0356
ISSN	0025-7931
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